抄録

Bacterial wilt caused by <i>Ralstonia solanacearum</i> is one of the most devastating plant diseases worldwide. <i>R. solanacearum</i> first invades intercellular spaces of roots where it multiplies before invading xylem vessels and producing exopolysaccharide (EPS), leading to wilt of the infected plant. In this review, we focus on regulation of <i>R. solanacearum</i> pathogenicity, which requires proliferation in intercellular spaces. <i>R. solanacearum</i> possesses <i>hrp</i> encoding the type III secretion system (T3SS), and its pathogenicity depends on interactions between the host plant and type III effectors. HrpB positively regulates expression of not only <i>hrp</i> but also genes encoding exoproteins secreted through the type II secretion system (T2SS). A consortium of T2SS-secreted exocellular proteins containing plant cell wall-degrading enzymes contributes to not only invasion of xylem vessels, leading to systemic infection, but also quantitative control of virulence. Moreover, T2SS functionally interacts with T3SS. PhcA activated by quorum sensing in response to the bacterial cell density induces expression of <i>xpsR</i>, leading to biosynthesis of EPS. Moreover, active PhcA also suppresses expression of <i>prhIR</i>, resulting in suppression of <i>hrp</i> expression. These results suggest that <i>R. solanacearum</i> pathogenicity is globally regulated by mutual regulation by pathogenicity factors through multiplication of the bacteria in intercellular spaces.